Rat Podocytes
Cat.No.: CSC-C9378W
Species: Rat
Source: Kidney
Morphology: Epithelial-like
Cell Type: Podocyte
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Rat podocytes, a primary glomerular cell type of rat kidney podocyte lines, have been used extensively as a model for kidney function and pathology. In the glomerulus, these visceral epithelial cells attach to the basement membrane surrounding the capillaries via branching protrusions in a sophisticated tertiary "foot" process network. These processes bundle together to make a slit diaphragm, which prevents the accumulation of proteins and other large molecules in the urine, keeping the structure of the glomerular filtration barrier intact.
The cytoskeleton of podocytes is rich in actin, allowing them to dynamically remodel and adapt to pressure changes. Their complex shape and molecular dynamics keep the flux of substances between blood and urine exactly under control, maintaining the internal environment. In immunofluorescence testing, podocyte markers can be identified including podocin, angiotensin 1, nephrin, actin 4, and NPHS2. In clinical research, rat podocyte lines play an essential role in the study of glomerular disease, especially diabetic nephropathy and membranous nephropathy. The lineages of in vitro cultured podocytes offer a robust model for understanding podocyte biology, molecular biology and drug discovery. They are also critical for examining cell signaling pathways, mechanisms of podocyte damage and therapeutic strategies, helping to uncover the underlying pathology of renal disease and experimentally supporting new therapies.
Fig. 1. Electron micrographs of rat podocyte foot processes. (a) Perpendicular sections. (b, d) Horizontal sections. (c) Cross-sections (Ichimura K, Kurihara H, et al., 2003).
Targeting tissue-resident memory CD8+ T cells in the kidney is a potential therapeutic strategy to ameliorate podocyte injury and glomerulosclerosis
Background
Renal tissue-resident memory T (TRM) cells were abundant in kidney, and CD8+ TRM cells increased in patients and mice with FSGS, diabetic kidney disease, and lupus nephritis. IL-15 promoted renal CD8+ TRM cell formation and activation, driving podocyte injury and glomerulosclerosis. Blocking IL-15/CD122 reduced TRM responses and renal injury. Sparsentan, a dual angiotensin II receptor/endothelin type A receptor antagonist, also inhibited IL-15-mediated CD8+ TRM responses. Targeting renal CD8+ TRM cells may offer a new therapeutic strategy for glomerular diseases.
Key Findings
1) Kidney contains abundant TRM cells; CD8+ TRM cells are significantly increased in human and murine FSGS, DKD, and LN, arising from peripheral CD69− memory T cells. 2) Renal IL-15 is elevated and correlates with proteinuria; IL-15 promotes CD8+ TRM cell formation and activation. 3) Anti-IL-15 or anti-CD122 antibody treatment inhibits renal CD8+ TRM cells, lowers proteinuria, and alleviates podocyte injury and glomerulosclerosis in ADR-treated and db/db mice, independent of NK cells. 4) Activated renal CD8+ TRM cells directly induce podocyte apoptosis, nephrin/podocin loss, cytoskeletal and mitochondrial damage. 5) Sparsentan reduces CD8+ TRM formation/activation and podocyte injury by inhibiting Ang II/ET-1-mediated IL-15 signaling.
Contribution
Creative Bioarray supplied the murine podocyte cell line (MPC) used in co-culture assays. This enabled evaluation of cytotoxic effects of renal CD8+ TRM cells on podocytes and protective effects of IL-15 blockade/Sparsentan, thereby supporting key mechanistic findings.
Moringa oleifera Leaf Extract Enhances the Viability and Inhibits Ferroptosis in High Glucose-induced Rat Podocytes
Diabetic nephropathy (DN) is a severe complication in patients with diabetes mellitus, which is mainly characterized by glomerular podocyte injury. Ferroptosis is crucial in the pathogenesis of DN. Moringa oleifera leaf extract (MOLE) has attracted attention due to its multiple pharmacological activities, but it is unclear whether it can delay the progression of DN by inhibiting ferroptosis.
DN model cells were established using rat podocytes induced by high glucose (HG); the cells were processed with MOLE, dapagliflozin (DAPA, positive control), and acyl-CoA synthetase long-chain family member 4 (ACSL4) overexpression plasmids. Cell viability, Fe2+ concentration, reactive oxygen species (ROS), malondialdehyde (MDA), and glutathione (GSH) levels were monitored.
MOLE treatment markedly enhanced HG-induced rat podocyte viability, decreased intracellular Fe2+ concentration, ROS level, MDA concentration, and elevated GSH concentration. ACSL4 overexpression reversed the protective effect of MOLE on podocytes. This finding provides a theoretical basis for further developing MOLE-based therapeutic agents for DN treatment.
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